Coronary artery disease and myocardial infarction may lead to major clinical problems of left ventricular dysfunction and arrhythmias. Both are common. Salvage of ischemic myocardium is directed toward the reversibly damaged "borderzone" tissue at the ischemic edge. Our recent laboratory and clinical investigations also incriminate this "borderzone" as the origin of ischemic cardiac arrhythmias. We propose to further examine the character and extent of the peri-ischemic "borderzone." Pyridine nucleotide fluorophotography will provide a high resolution indicator of mitochondrial function at the ischemic edge. Four pharmacologic agents will be tested as prototypic infarct size modifers: a) decrease myocardial oxygen demand (propranolol), b) steroids (methylprednisolone), c) oxygen diffusion facilitator (hyaluronidase) and d) calcium antagonist (nifedipine). The peri-ischemic "borderzone" also appears to harbor the slow conducting tissue that is the requisite substrate of re-entrant ventricular tachyarrhythmias. Three surgical techniques are currently employed to ablate the arrhythmia circuit: cryosurgery, encircling ventriculotomy and endocardial excision. Each of these surgical procedures must heal with scar leaving a transition zone between scar and normal myocardium. We propose to further examine this transition zone and the peri-ischemic "borderzone" relative to current flux, extracellular and intracellular resistivity, refractoriness and electrogram configuration.